Lum, also known as lumican, is a member of the small leucine-rich proteoglycan family. It plays roles in various biological processes and is involved in extracellular matrix-related pathways [2,3,4]. Its functions may be related to cell proliferation regulation and the inflammatory response [4]. Genetic models, such as mouse models, can be useful in studying Lum's functions.

In calcific aortic valve disease (CAVD), single-cell RNA-sequencing (scRNA-seq) characterized the pathological switch process of valve interstitial cells (VICs). The pro-calcification role of LUM was confirmed in vitro, ex vivo, in vivo, and in ApoE -/-//LUM -/- double knockout mice. LUM induces osteogenesis in VICs via activation of inflammatory pathways and augmentation of cellular glycolysis, leading to lactate accumulation and histone lactylation, which facilitates valve calcification [1].

In gastric cancer, LUM expression was higher in cancer tissues compared to adjacent non-tumor tissues. High LUM expression was correlated with tumor differentiation, T stage, and pathological stage, and patients with high LUM expression had a poor prognosis. Gene set enrichment analysis indicated that 14 signaling pathways were enriched in samples with high-LUM expression phenotype [2].

In non-alcoholic fatty liver disease (NAFLD), LUM was identified as the hub gene of advanced fibrosis through weighted gene co-expression network analysis (WGCNA), and the identified module was related to the extracellular matrix, cell proliferation regulation, and the inflammatory response [4].

In conclusion, Lum plays important roles in diseases such as CAVD, gastric cancer, and NAFLD. Gene-knockout mouse models, like the ApoE -/-//LUM -/- double knockout mice in CAVD research, have revealed its pro-calcification role, contributing to understanding the disease mechanisms. In gastric cancer, its role as an oncogene and in NAFLD as a hub gene for advanced fibrosis also highlight its significance in these disease areas.